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Lack of Albumin as Genotypic Marker of Preneoplastic Analbuminemic Rat Hepatocytes Transplanted within Albumin-positive Liver¹

Department of Pathology, Sapporo Medical College [K. Y., K. O., M. M.], S. I, W. 17, Chuo-ku, Sapporo 060; and Department of Chemistry, Sasaki Institute [S. M.], 2-2 Kanda Surugadai, Chiyoda-ku, Tokyo 101, Japan

In analbuminemic rats, preneoplastic hepatocytes lack the capability to produce albumin. On the other hand, the hepatocytes of F1 hybrids born from parents of analbuminemic rats and normal rats retain their capability to produce albumin, since the analbuminemia is inherited as a recessive trait in rats. We isolated hyperplastic nodule cells from Nagase's analbuminemic rats and transplanted them into the livers of F1 hybrid rats by infusion into the mesenteric vein. The host rats were subjected to a short term dietary 2-acetylaminofluorene and underwent a two-thirds partial hepatectomy to promote the growth of preneoplastic hepatocytes. Within 10 to 13 days after transplantation, many albuminnegative hepatocytic nodules were formed in the albumin-positive host livers. Almost all the albumin-negative nodules expressed conventional biochemical markers for preneoplastic hepatocytes. Eight to 9 weeks after the transplantation, almost the same number of albumin-negative nodules were observed as on days 10–13. However, roughly a half of the albumin-negative nodules showed no biochemical markers. The results indicate that the majority of early preneoplastic lesions revert to become phenotypically normal after removal of the promoting stimuli.

¹ Supported by a grant from the Ministry of Education, Culture and Science of Japan and from the Hokkaiddo Society of Promotion of Gerontology.

² To whom requests for reprints should be addressed.

Received 7/14/87. Revised 10/13/87. Accepted 10/16/87.